Rituximab (anti-CD20) has become first-line therapy for moderate-to-severe pemphigus vulgaris. The primary mechanism by which rituximab induces remission in pemphigus is:

• A Depleting plasma cells directly to eliminate anti-DSG antibody production
• B Blocking FcRn receptor to accelerate IgG catabolism
• C Depleting CD20+ B-cells (including autoreactive B-cell precursors) thereby reducing autoantibody production long-term ✓
• D Inducing regulatory T-cells that suppress anti-DSG autoimmunity

Explanation

Rituximab depletes CD20+ B-cells (naïve, memory, and transitional B-cells), thereby eliminating autoreactive B-cell clones that differentiate into plasmablasts producing anti-desmoglein-1 and anti-desmoglein-3 IgG. The sustained remission after rituximab (often 12–18 months) reflects depletion of memory B-cells; plasma cells lack CD20 and are not directly depleted. FcRn blockade is the mechanism of FcRn inhibitors (rozanolixizumab, efgartigimod) — a different drug class.

Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.